|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Collectively, the present results suggest that in the treatment of leukemia, taxodione has potential as a compound with high efficacy to overcome BCR-ABL T315I mutation-mediated resistance in leukemia cells.
|
29859988 |
2018 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
T315I mutation of BCR-ABL1 into human Philadelphia chromosome-positive leukemia cell lines by homologous recombination using the CRISPR/Cas9 system.
|
29967475 |
2018 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Antitumor Effects of Blocking Protein Neddylation in T315I-BCR-ABL Leukemia Cells and Leukemia Stem Cells.
|
29321163 |
2018 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Ponatinib-Induced Graft-versus-Host Disease/Graft-versus-Leukemia Effect in a Patient with Philadelphia-Positive Acute Lymphoblastic Leukemia without the T315I Mutation Relapsing after Allogeneic Transplant.
|
28810255 |
2017 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Surprisingly, inhibition of AurA by AKI603 induced leukemia cell senescence in both BCR-ABL wild type and T315I mutation cells.
|
27824120 |
2016 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
In BCR/ABL- or BCR/ABL-T315I-driven murine leukemia as well as in xenograft models of primary Ph+ leukemia harboring the T315I, PF-114 significantly prolonged survival to a similar extent as ponatinib.
|
25394714 |
2015 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Here we combine comprehensive drug sensitivity and resistance profiling of patient cells ex vivo with structural analysis to establish the VEGFR tyrosine kinase inhibitor axitinib as a selective and effective inhibitor for T315I-mutant BCR-ABL1-driven leukaemia.
|
25686603 |
2015 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Ponatinib is the only currently approved tyrosine kinase inhibitor (TKI) that suppresses all BCR-ABL1 single mutants in Philadelphia chromosome-positive (Ph(+)) leukemia, including the recalcitrant BCR-ABL1(T315I) mutant.
|
25132497 |
2014 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
MK-0457 has important activity in patients with leukemias expressing the highly resistant T315I BCR-ABL mutation.
|
22772060 |
2013 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
One mutation, T315I, for example, renders the leukemia resistant to all first- and second-line TKIs.
|
23666688 |
2013 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Given the fact that all AKIs fail to inhibit BCR/ABL harboring the 'gatekeeper' mutation T315I, we investigated the effects of AKIs in combination with the allosteric inhibitor GNF2 in Ph + leukemia.
|
22985168 |
2012 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Allogeneic stem cell transplantation for patients harboring T315I BCR-ABL mutated leukemias.
|
21926354 |
2011 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Although many imatinib-resistant mutations respond well to second-generation TKIs, the threonine-to-isoleucine mutation at codon 315 of the breakpoint cluster region/v-abl Abelson murine leukemia viral oncogene protein fusion Bcr-Abl (T315I) is insensitive to all currently available TKIs.
|
20564073 |
2010 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Although strategies to overcome resistance-mediated T315I mutation may improve the survival of BCR-ABL-positive leukemia patients, there is little information on cell-based studies.
|
20471447 |
2010 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
KW-2449, a multikinase inhibitor of FLT3, ABL, ABL-T315I, and Aurora kinase, is under investigation to treat leukemia patients.
|
19541823 |
2009 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Some emerging aurora kinase inhibitors, such as VX-680, PHA-739358, MK-0457 and AS703569, and Smo1 and Hedgehog (Hh) inhibitors promise clinical efficacy against the Bcr-Ab T315I mutant form and leukaemia stem cells, respectively.
|
19959093 |
2009 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
More importantly, ON012380 was found to induce apoptosis of all of the known imatinib-resistant mutants at concentrations of <10 nM concentration in vitro and cause regression of leukemias induced by i.v. injection of 32Dcl3 cells expressing the imatinib-resistant BCR-ABL isoform T315I.Daily i.v. dosing for up to 3 weeks with a >100 mg/kg concentration of this agent is well tolerated in rodents, without any hematotoxicity.
|
15677719 |
2005 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
The resistance to the tyrosine kinase inhibitor imatinib in BCR/ABL-positive leukemias is mostly associated with mutations in the kinase domain of BCR/ABL, which include the most prevalent mutations E255K and T315I.
|
15194504 |
2004 |